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degeneration

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As with most chronic degenerative kidney diseases, the gradual decline of renal function at later stages of DNP is invariably associated with tubular epithelial degeneration (TED), also called tubular atrophy, and interstitial fibrosis (IF), hallmarks of degeneration to end-stage renal failure [3].

The mitochondrial vacuolation could in part be the result of persistent mitochondrial dysfunction and further facilitate the downstream motor neuron degeneration events.

is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [ 8 ] . Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [ 9 10 11 ] . Control of thin filament length is critical for maintaining proper sarcomere function and length [ 12 ] . Inhibition of Tmod1's capping activity - either by using an antibody to its C-terminal end or by decreasing expression using an antisense Tmod1 transcript - results in elongated thin filaments and decreased cardiac contractility [ 13 14 ] . Tmod1 overexpression in rat cardiomyocytes causes shortening of the thin filaments and sarcomere disorganization, resulting in myofibril degeneration [ 14 ] . Likewise, mice overexpressing TMOD1 in the heart show disrupted sarcomere organization with shortened thin filaments, leading to myofibril degeneration and dilated cardiomyopathy [ 15 ] . Recently, Littlefield and colleagues showed that overexpression of GFP-Tmod1 in chick cardiac myocytes results in shortening of thin filaments; the authors proposed that excess Tmod1 decreases the affinity between actin monomers and pointed ends, leading to monomer dissociation and filament shortening [ 42 ] . Mutations in many proteins making up the cardiac sarcomere have been shown to cause cardiac hypertrophy [ 16 17 18 19 ] :mutations in the TPM1 gene, for example, cause type 3 familial hypertrophic cardiomyopathy (CMH3), and a transgenic mouse expressing a CMH3 mutation develops ventricular myocyte disarray and hypertrophy [ 20 ] . Mutations in myosin heavy chain 7 are estimated to account for 40-50% of the cases of hypertrophic cardiomyopathy [ 21 ] .

Fibers in "advanced transition" (rows 3 and 4), and those undergoing degeneration (rows 6 and 7), are associated with cytoplasmic p27 expression.

Thus, MVISE represents a previously uncharacterized mechanism of mitochondrial degeneration in the CNS.